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Rosiglitazone Abrogates Bleomycin-Induced …

Matrix PathobiologyRosiglitazone Abrogates bleomycin -InducedScleroderma and Blocks profibrotic ResponsesThrough peroxisome proliferator -ActivatedReceptor- Minghua Wu, Denisa S. Melichian, Eric Chang,Matthew Warner-Blankenship, Asish K. Ghosh,and John VargaFrom the Section of Rheumatology, Northwestern UniversityFeinberg School of Medicine, Chicago, IllinoisThe nuclear hormone receptor, peroxisome prolif-erator-activated receptor (PPAR)- , originally iden-tified as a key mediator of adipogenesis, is ex-pressed widely and implicated in diverse natural and synthetic agonists ofPPAR- abrogated the stimulation of collagen synthe-sis and myofibroblast differentiation induced bytransforming growth factor (TGF)- in vitro. To char-acterize the role of PPAR- in the fibrotic processinvivo, the synthetic agonist Rosiglitazone was used in amouse model of scleroderma .

Matrix Pathobiology Rosiglitazone Abrogates Bleomycin-Induced Scleroderma and Blocks Profibrotic Responses Through Peroxisome Proliferator-Activated

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  Response, Through, Induced, Bleomycin, Scleroderma, Rosiglitazone abrogates bleomycin induced, Rosiglitazone, Abrogates, Rosiglitazone abrogates bleomycin induced scleroderma, Profibrotic responses through peroxisome proliferator, Profibrotic, Peroxisome, Proliferator

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